Transfer of immunity to Babesia microti of human origin using T lymphocytes in mice

Ruebush, Mary J.; Hanson, William L.

doi:10.1016/0008-8749(80)90347-0

Cited by 32 publications

(14 citation statements)

References 20 publications

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“…While studies have demonstrated an important role for T cells in controlling parasitemia, studies in SCID mice have suggested that innate immunity may be of primary importance (16, 30, 47-49). Our results, along with available literature, are consistent with a model in which innate immunity is progressively activated during infection to kill parasites within infected erythrocytes.…”

Section: Discussionmentioning

confidence: 99%

Elimination of Babesia microti Is Dependent on Intraerythrocytic Killing and CD4+ T Cells

Skariah

Arnaboldi

Dattwyler

et al. 2017

The Journal of Immunology

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Babesiosis is a tick-borne zoonosis caused by protozoans of the genus Babesia; apicomplexan parasites that replicate within erythrocytes. However, unlike related Plasmodium species, the pathogenesis of Babesia infection remains poorly understood. The primary etiological agent of babesiosis in the US is B. microti. In healthy individuals, tick transmitted infection with Babesia causes no specific clinical manifestations, with many having no symptoms at all. However, even in asymptomatic people, a Babesia carriage state can be established that can last up to a year or more. Current blood bank screening methods do not identify infected donors, and Babesia parasites survive blood banking procedures and storage. Thus, Babesia can also be transmitted by infected blood, and is currently the number one cause of reportable transfusion transmitted infection in the US. Despite a significant impact on human health, B. microti remains understudied. Here, we evaluated the course of Babesia infection in three different strains of mice, C57BL/6J, BALB/cJ and C3H-HeJ, and examined the contribution of multiple immune parameters including: toll-like receptors, B cells, CD4+ cells, IFN-γ, and nitric oxide on the level of parasitemia and parasite clearance during acute babesiosis. We found that B. microti reaches high parasitemia levels during the first week of infection in all three mice strains before resolving spontaneously. Our results indicate that resolution of babesiosis requires CD4 T cells and a novel mechanism of parasite killing within infected erythrocytes.

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Section: Discussionmentioning

confidence: 99%

Elimination of Babesia microti Is Dependent on Intraerythrocytic Killing and CD4+ T Cells

Skariah

Arnaboldi

Dattwyler

et al. 2017

The Journal of Immunology

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“…In fact, it is possible to protect mice from Babesia infections by the adoptive transfer of spleen cells from immune animals (127,128,182,242). Moreover, good levels of protection seem to be conferred specifically by splenocytes and not by lymph node cells (194), probably reflecting the fact that the systemic antigens are channeled preferentially to the spleen and not to peripheral lymph nodes.…”

Section: Host Immune Responsementioning

confidence: 99%

“…T cells have also been implicated in the protection against lethal Babesia species; mice immunized against B. rodhaini experience a rising parasitemia and high mortality when treated with antithymocyte serum (244). Further, it has been shown that the transfer of purified T lymphocytes obtained from immune animals is sufficient to confer immunity to B. microti in naive mice (194), and the adoptive transfer of immune thymocytes to immunodeficient mice confers the ability to resolve a B. microti infection (123) (Fig. 3C).…”

Section: Host Immune Responsementioning

confidence: 99%

Babesiosis

Homer¹,

Aguilar-Delfín²,

Telford³

et al. 2000

Clinical Microbiology Reviews

522

402

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Section: Introductionmentioning

confidence: 99%

“…1968) and it has been suggested that this was due to the transfer of sensitised T cells (Reubush and Hanson, 1980). Reubush and Hanson (1980) further suggested that these sensitised T cells could act by modulating the secretion by macrophages of non-specific factors toxic for the parasite. However, recent experiments have strongly implicated antibodies produced by sensitised B cells as responsible for the adoptive transfer of immunity to B. microti (Meeusen, Lloyd and Soulsby, 1984).…”

Section: Introductionmentioning

confidence: 99%

BABESIA MICROTI IN MICE. SUBPOPULATIONS OF CELLS INVOLVED IN THE ADOPTIVE TRANSFER OF IMMUNITY WITH IMMUNE SPLEEN CELLS

Meeusen

Lloyd

Soulsby

1984

Aust J Exp Biol Med

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Summary Protection against a primary Babesia microti infection in mice, induced by the adoptive transfer of immune spleen cells, was abolished when the immune spleen cells were treated with mitomycin C prior to transfer. Since mitomycin C treatment prevents the replication of lymphocytes without affecting other cell functions, these results would suggest that the transferred cells required proliferation in the recipient mice before they could exert their protective effect, and this excludes the already differentiated antibody‐forming cells (AFC's), macrophages and sensitised helper T cells. This was partly supported by the finding that Sephadex G‐10 non‐adherent immune cells, depleted of macrophages and AFC's, still conferred a strong protection after transfer. However, the Sephadex G‐10 adherent cells, on a cell to cell basis, initially conferred a better protection against B. microti than did the non‐adherent cells or unfractionated immune spleen cells. The possibility of the retention of an intermediate B memory cell type on the Sephadex G‐10 columns and the suppression of antibody production are discussed in view of these results.

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Transfer of immunity to Babesia microti of human origin using T lymphocytes in mice

Cited by 32 publications

References 20 publications

Elimination of Babesia microti Is Dependent on Intraerythrocytic Killing and CD4+ T Cells

Elimination of Babesia microti Is Dependent on Intraerythrocytic Killing and CD4+ T Cells

Babesiosis

BABESIA MICROTI IN MICE. SUBPOPULATIONS OF CELLS INVOLVED IN THE ADOPTIVE TRANSFER OF IMMUNITY WITH IMMUNE SPLEEN CELLS

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